AJP - Endocrinology and Metabolism, Vol 257, Issue 6 E879-E884, Copyright © 1989 by American Physiological Society
Stimulation of plasma inactive renin by dexamethasone in the cat
N. Glorioso, C. Troffa, G. Tonolo, M. G. Melis, P. Manunta, A. Soro, P. Madeddu, A. Pazzola and F. Pala
Centro Ipertensione, Patologia Medica, University of Sassari, Italy.
An inactive form of renin in human plasma is the biosynthetic precursor,
prorenin. The cat is a good animal model for studies of inactive renin. The
gene for human renin contains sequences homologous to the glucocorticoid
consensus sequence. The response of cat plasma (active and inactive renin)
and of angiotensinogen to administration of dexamethasone (0.5 mg/kg im,
daily) was studied in ketamine-sedated cats (20 mg/kg im). Inactive renin
increased by twofold after 7 days of dexamethasone (P less than 0.01).
After a 7-day recovery period, it returned to base line. Active renin did
not change. Angiotensinogen fell by 35% (P less than 0.01). The time course
of the selective increase of plasma inactive renin showed that inactive
renin began to rise after 2 days, peaking after 5 days. Ketamine alone
induced inactive renin to rise slightly but significantly (P less than
0.05), although the magnitude of the increment was much less than that
observed in ketamine-sedated cats receiving dexamethasone (P less than
0.01). Active renin did not change, whereas angiotensinogen was reduced by
25% (P less than 0.01). Our findings support the hypothesis that
glucocorticoids might have a selective role in the synthesis and/or
secretion of the precursor of renin, at least in the cat.
